首页> 外文期刊>Chinese Medical Journal >INCREASED VULNERABILITY OF HYPERTROPHIED MYOCARDIUM TO ISCHEMIA AND REPERFUSION INJURY: RELATION TO CARDIAC RENIN-ANGIOTENSIN SYSTEM
【24h】

INCREASED VULNERABILITY OF HYPERTROPHIED MYOCARDIUM TO ISCHEMIA AND REPERFUSION INJURY: RELATION TO CARDIAC RENIN-ANGIOTENSIN SYSTEM

机译:心肌肥大对缺血和再灌注损伤的易感性:与心脏肾素-血管紧张素系统的关系

获取原文
获取原文并翻译 | 示例
           

摘要

Hearts of pressure-overload hypertrophy show an increased activation of intracardiac renin angiotensin system which may contribute to ischemia and reperfusion injury. The purpose of this study is to evaluate whether the hypertrophied myocardium is more vulnerable to ischemia and reperfusion injury and to find out its relation to the cardiac renin-angiotensin system. Hypertrophied rat hearts induced by abdominal aortic banding for 6 weeks were subjected to 2 hours of hypothermic ischemic arrest followed by 30 minutes of reperfusion, and their cardiac function recovery was compared with that of sham—operated normal control hearts. The cardiac renin activity and angiotensin Ⅱ content before ischemia and after reperfusion were determined. It was found that both the pre—ischemic renin activity and angiotensin Ⅱ level were higher in hypertrophied myocardium than those in the control: ischemia and reperfusion injury increased both renin activity and angiotensin Ⅱ content in the two groups, but the renin activity and angiotensin Ⅱ level were further elevated after reperfusion in the hypertrophied hearts than those in the control hearts. Meanwhile, the cardiac function recovery after 30 minutes reperfusion in the hypertrophied hearts was poorer than that in the control. Correlation analysis revealed that there was a negative correlation between the cardiac output recovery and the myocardial angiotensin Ⅱ content (r = -0.8411, P < 0.001). It is concluded that ischemia and reperfusion injury can activate cardiac renin—angiotensin system in isolated rat heart, which may be responsible for the increased susceptibility of the hypertrophied myocardium to ischemia and reperfusion injury.
机译:压力超负荷肥大的心脏显示出心脏内肾素血管紧张素系统的激活增加,这可能导致局部缺血和再灌注损伤。这项研究的目的是评估肥大的心肌是否更易于缺血和再灌注损伤,并找出其与心脏肾素-血管紧张素系统的关系。将由腹主动脉束缚诱导的肥大大鼠心脏持续6周,进行2小时的低温缺血性停搏,然后再灌注30分钟,并将其心脏功能恢复与假手术的正常对照心脏进行比较。测定缺血前和再灌注后的心脏肾素活性和血管紧张素Ⅱ含量。发现肥厚型心肌缺血前肾素活性和血管紧张素Ⅱ水平均高于对照组:缺血和再灌注损伤使两组的肾素活性和血管紧张素Ⅱ含量均增加,但肾素活性和血管紧张素Ⅱ肥厚性心脏再灌注后血钙水平进一步高于对照组。同时,肥厚型心脏再灌注30分钟后的心功能恢复较对照组差。相关分析表明,心输出量恢复与心肌血管紧张素Ⅱ含量呈负相关(r = -0.8411,P <0.001)。结论是缺血和再灌注损伤可以激活离体大鼠心脏的心脏肾素-血管紧张素系统,这可能是肥大心肌对缺血和再灌注损伤的敏感性增加的原因。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号